Abstract
Polyamine synthesis and abnormal regulation of B cell differentiation occur concurrently in various diseases. We investigated whether putrescine could suppress germinal center B cell (GCB) differentiation by inducing reactive oxygen species (ROS) generation. The results of flow cytometry analysis revealed that putrescine did not affect B cell apoptosis and cell cycle. The results of RT-qPCR and western blotting revealed that putrescine could inhibit CD79a phosphorylation rather than total expression. Using an O2K high-resolution respirometer, we illustrated that putrescine increased the oxygen consumption rate in the basal mitochondrial respiration stage, ATP-coupled respiration stage, and maximum respiration stage. Similarly, it also elevated ROS generation across stages in B cells and reduced the proportion of GCB cells. Meanwhile, ROS scavenging by SOD could reverse such inhibitory effects on GCB cells. We concluded that putrescine could inhibit the differentiation of GCB cells by reducing CD79a phosphorylation and increasing ROS levels in GCB cells.